Pulmonary hypertensive vasculopathy in parenchymal lung diseases and/or hypoxia

Ghigna, Maria Rosa; Mooi, Wolter J.; Grünberg, Katrien

doi:10.1183/16000617.0003-2017

Cited by 14 publications

(12 citation statements)

References 110 publications

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“…Although tissue has been considered the standard material for molecular analyses, small pleural biopsies and cytology fluid specimens are the only material available in almost 80% of cases. 62 Moreover, the concordance between the primary tumor and pleural metastases concerning mutational alterations is very high. 63 Therefore, PF samples (CBs, smears, cytospins or liquid-based cytology) are considered suitable alternatives to tissue biopsy for molecular studies, provided they are not paucicellular.…”

Section: Biomarkers Of Malignant Effusionsmentioning

confidence: 99%

Biomarkers in the diagnosis of pleural diseases: a 2018 update

Porcel

2018

Ther Adv Respir Dis

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The use of biomarkers on pleural fluid (PF) specimens may assist the decision-making process and enhance clinical diagnostic pathways. Three paradigmatic examples are heart failure, tuberculosis and, particularly, malignancy. An elevated PF concentration of the amino-terminal fragment of probrain natriuretic peptide (>1500 pg/ml) is a hallmark of acute decompensated heart failure. Adenosine deaminase, interferon-γ and interleukin-27 are three valuable biomarkers for diagnosing tuberculous pleurisy, yet only the first has been firmly established in clinical practice. Diagnostic PF biomarkers for malignancy can be classified as soluble-protein based, immunocytochemical and nucleic-acid based. Soluble markers (e.g. carcinoembryonic antigen (CEA), carbohydrate antigen 15–3, mesothelin) are only indicative of cancer, but not confirmatory. Immunocytochemical studies on PF cell blocks allow: (a) to distinguish mesothelioma from reactive mesothelial proliferations (e.g. loss of BAP1 nuclear expression, complemented by the demonstration of p16 deletion using fluorescence in situ hybridization, indicate mesothelioma); (b) to separate mesothelioma from adenocarcinoma (e.g. calretinin, CK 5/6, WT-1 and D2-40 are markers of mesothelioma, whereas CEA, EPCAM, TTF-1, napsin A, and claudin 4 are markers of carcinoma); and (c) to reveal tumor origin in pleural metastases of an unknown primary site (e.g. TTF-1 and napsin A for lung adenocarcinoma, p40 for squamous lung cancer, GATA3 and mammaglobin for breast cancer, or synaptophysin and chromogranin A for neuroendocrine tumors). Finally, PF may provide an adequate sample for analysis of molecular markers to guide patients with non-small cell lung cancer to appropriate targeted therapies. Molecular testing must include, at least, mutations of epidermal growth-factor receptor and BRAF V600E, translocations of rat osteosarcoma and anaplastic lymphoma kinase, and expression of programmed death ligand 1.

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Section: Biomarkers Of Malignant Effusionsmentioning

confidence: 99%

Biomarkers in the diagnosis of pleural diseases: a 2018 update

Porcel

2018

Ther Adv Respir Dis

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“…Abnormalities of the pulmonary vessels are commonly seen across a number of pulmonary diseases, including chronic obstructive pulmonary disease (COPD), asthma, idiopathic pulmonary fibrosis, bronchiectasis and others [1][2][3][4]. For individuals with these conditions, the development of overt pulmonary vascular disease (known as Group 3 pulmonary hypertension in the World Health Organization classification scheme [5]) is a major clinical inflection point that predicts future morbidity and mortality [6][7][8][9][10]. It is likely that mild perturbations in the pulmonary vascular system, even below traditional thresholds of disease, are associated with poor outcomes [11,12].…”

Section: Introductionmentioning

confidence: 99%

Radiographic pulmonary vessel volume, lung function and airways disease in the Framingham Heart Study

Synn

Estépar

et al. 2019

Eur Respir J

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Radiographic abnormalities of the pulmonary vessels, such as vascular pruning, are common in advanced airways disease, but it is unknown if pulmonary vascular volumes are related to measures of lung health and airways disease in healthier populations.In 2388 participants of the Framingham Heart Study computed tomography (CT) sub-study, we calculated total vessel volumes and the small vessel fraction using automated CT image analysis. We evaluated associations with measures of lung function, airflow obstruction on spirometry and emphysema on CT. We further tested if associations of vascular volumes with lung function were present among those with normal forced expiratory volume in 1 s and forced vital capacity.In fully adjusted linear and logistic models, we found that lower total and small vessel volumes were consistently associated with worse measures of lung health, including lower spirometric volumes, lower diffusing capacity and/or higher odds of airflow obstruction. For example, each standard deviation lower small vessel fraction (indicating more severe pruning) was associated with a 37% greater odds of obstruction (OR 1.37, 95% CI 1.11–1.71, p=0.004). A similar pattern was observed in the subset of participants with normal spirometry.Lower total and small vessel pulmonary vascular volumes were associated with poorer measures of lung health and/or greater odds of airflow obstruction in this cohort of generally healthy adults without high burdens of smoking or airways disease. Our findings suggest that quantitative CT assessment may detect subtle pulmonary vasculopathy that occurs in the setting of subclinical and early pulmonary and airways pathology.

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“…The main mechanism of PH in ILD is due to parenchymal fibrosis and vascular bed destruction, although other concomitant factors can exist, including venous thromboembolism, sleep-disordered breathing, and left heart dysfunction with postcapillary PH. 31 , 32 , 33 , 34 The only approved pharmacologic therapies for treating IPF are the antifibrotic agents pirfenidone and nintedanib, which slow the rate of disease progression but have shown no effect on the development or progression of pulmonary vascular disease.…”

Section: Pulmonary Hypertension Associated With Interstitial Lung Diseasesmentioning

confidence: 99%

Management of Pulmonary Hypertension Due to Chronic Lung Disease

Sugarman

Weatherald

2021

Methodist DeBakey Cardiovascular Journal

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Pulmonary hypertension (PH) is a known complication of chronic parenchymal lung diseases, including chronic obstructive lung disease, interstitial lung diseases, and more rare parenchymal lung diseases. Together, these diseases encompass two of the five clinical classifications of PH: group 3 (chronic lung disease [CLD] and/or hypoxia) and group 5 (unclear and/or multifactorial mechanisms). The principal management strategy in PH associated with CLD is optimization of the underlying lung disease. There has been increasing interest in therapies that treat pulmonary arterial hypertension (group 1, PAH), and although some studies have explored the use of these oral PAH-targeted therapies to treat PH associated with CLD , there is currently no evidence to support their routine use; in fact, some studies suggest harm. Inhaled therapies that target the pulmonary vasculature may avoid certain problems observed with oral PAH therapies. Recent studies suggest a promising role for inhaled PAH therapies in group 3 PH, but this requires further study. The objective of this article is to review the current treatment strategies for group 3 and group 5 PH.

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Pulmonary hypertensive vasculopathy in parenchymal lung diseases and/or hypoxia

Cited by 14 publications

References 110 publications

Biomarkers in the diagnosis of pleural diseases: a 2018 update

Biomarkers in the diagnosis of pleural diseases: a 2018 update

Radiographic pulmonary vessel volume, lung function and airways disease in the Framingham Heart Study

Management of Pulmonary Hypertension Due to Chronic Lung Disease

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